Recognition of YKL-39, a human cartilage related protein, as a target antigen in patients with rheumatoid arthritis
- aRheumatology, Immunology and Genetics Programme, Institute of Medical Science, St Marianna University, School of Medicine 2–16–1, Sugao, Miyamae-ku, Kawasaki, Kanagawa, 216–8512, Japan, bMitsubishi Kagaku Bio-Clinical Laboratories Inc, 3–30–1, Shimura, Itabashi-ku, Tokyo, 174-8555, Japan, cDepartment of Orthopaedic Surgery, Okayama University School of Medicine, 2–5–1, Shikata-cho, Okayama, 700-8558, Japan, dDepartment of Biochemistry and Molecular Dentistry, Okayama University Dental School, 2–5–1, Shikata-cho, Okayama, 700–8558, Japan
- Dr Katorigplken{at}air.linkclub.or.jp
- Accepted 26 April 2000
Abstract
OBJECTIVE To investigate whether autoimmunity to YKL-39, a recently cloned cartilage protein, occurs in patients with rheumatoid arthritis (RA).
METHODS Autoantibody to YKL-39 was assayed by enzyme linked immunosorbent assay (ELISA) and western blotting in serum samples from patients with RA, systemic lupus erythematosus (SLE), and healthy donors, using recombinant YKL-39 protein. This reactivity was compared with that against a YKL-39 homologue, YKL-40 (human cartilage gp-39/chondrex), which has been reported to be an autoantigen in RA.
RESULTS Autoantibody to YKL-39 was detected in seven of 87 patients with RA (8%), but not in serum samples from patients with SLE or healthy donors. YKL-40 reactivity was found in only one of 87 RA serum samples (1%), with no cross reactivity to YKL-39.
CONCLUSION The existence of anti-YKL-39 antibody in a subset of patients with RA is reported here for the first time. Further, it was shown that the immune response to YKL-39 was independent of that to YKL-40. Clarification of the antibody and T cell responses to autoantigens derived from chondrocyte, cartilage, or other joint components may lead to a better understanding of the pathophysiology of joint destruction in patients with RA.
